Difference between revisions of "Phielix 2010 Diabetologia"
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|title=Phielix E, Meex R, Moonen-Kornips E, Hesselink MK, Schrauwen P (2010) Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals. Diabetologia 53: 1714- | |title=Phielix E, Meex R, Moonen-Kornips E, Hesselink MK, Schrauwen P (2010) Exercise training increases mitochondrial content and ''ex vivo'' mitochondrial function similarly in patients with type 2 diabetes and in control individuals. Diabetologia 53:1714-21. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/20422397 PMID:20422397] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/20422397 PMID: 20422397 Open Access] | ||
|authors=Phielix E, Meex R, Moonen-Kornips E, Hesselink MK, Schrauwen P | |authors=Phielix E, Meex R, Moonen-Kornips E, Hesselink MK, Schrauwen P | ||
|year=2010 | |year=2010 | ||
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|abstract='''AIMS/HYPOTHESIS:''' We previously showed that type 2 diabetic patients are characterised by compromised intrinsic mitochondrial function. Here, we examined if exercise training could increase intrinsic mitochondrial function in diabetic patients compared with control individuals. | |abstract='''AIMS/HYPOTHESIS:''' We previously showed that type 2 diabetic patients are characterised by compromised intrinsic mitochondrial function. Here, we examined if exercise training could increase intrinsic mitochondrial function in diabetic patients compared with control individuals. | ||
'''METHODS:''' Fifteen male type 2 diabetic patients and 14 male control individuals matched for age, BMI and VO(2max) enrolled in a 12 week exercise intervention programme. Ex vivo mitochondrial function was assessed by high-resolution respirometry in permeabilised muscle fibres from vastus lateralis muscle. Before and after training, insulin-stimulated glucose disposal was examined during a hyperinsulinaemic-euglycaemic clamp. | '''METHODS:''' Fifteen male type 2 diabetic patients and 14 male control individuals matched for age, BMI and VO(2max) enrolled in a 12 week exercise intervention programme. ''Ex vivo'' mitochondrial function was assessed by high-resolution respirometry in permeabilised muscle fibres from vastus lateralis muscle. Before and after training, insulin-stimulated glucose disposal was examined during a hyperinsulinaemic-euglycaemic clamp. | ||
'''RESULTS:''' Diabetic patients had intrinsically lower ADP-stimulated state 3 respiration and lower carbonyl cyanide 4-(trifluoro-methoxy)phenylhydrazone (FCCP)-induced maximal oxidative respiration, both on glutamate and on glutamate and succinate, and in the presence of palmitoyl-carnitine (p < 0.05). After training, diabetic patients and control individuals showed increased state 3 respiration on the previously mentioned substrates (p < 0.05); however, an increase in FCCP-induced maximal oxidative respiration was observed only in diabetic patients (p < 0.05). The increase in mitochondrial respiration was accompanied by a 30% increase in mitochondrial content upon training (p < 0.01). After adjustment for mitochondrial density, state 3 and FCCP-induced maximal oxidative respiration were similar between groups after training. Improvements in mitochondrial respiration were paralleled by improvements in insulin-stimulated glucose disposal in diabetic patients, with a tendency for this in control individuals. | '''RESULTS:''' Diabetic patients had intrinsically lower ADP-stimulated state 3 respiration and lower carbonyl cyanide 4-(trifluoro-methoxy)phenylhydrazone (FCCP)-induced maximal oxidative respiration, both on glutamate and on glutamate and succinate, and in the presence of palmitoyl-carnitine (''p'' < 0.05). After training, diabetic patients and control individuals showed increased state 3 respiration on the previously mentioned substrates (''p'' < 0.05); however, an increase in FCCP-induced maximal oxidative respiration was observed only in diabetic patients (''p'' < 0.05). The increase in mitochondrial respiration was accompanied by a 30% increase in mitochondrial content upon training (''p'' < 0.01). After adjustment for mitochondrial density, state 3 and FCCP-induced maximal oxidative respiration were similar between groups after training. Improvements in mitochondrial respiration were paralleled by improvements in insulin-stimulated glucose disposal in diabetic patients, with a tendency for this in control individuals. | ||
'''CONCLUSIONS/INTERPRETATION:''' We confirmed lower intrinsic mitochondrial function in diabetic patients compared with control individuals. Diabetic patients increased their mitochondrial content to the same extent as control individuals and had similar intrinsic mitochondrial function, which occurred parallel with improved insulin sensitivity. | '''CONCLUSIONS/INTERPRETATION:''' We confirmed lower intrinsic mitochondrial function in diabetic patients compared with control individuals. Diabetic patients increased their mitochondrial content to the same extent as control individuals and had similar intrinsic mitochondrial function, which occurred parallel with improved insulin sensitivity. | ||
|keywords= | |keywords=Type 2 diabetes, Insulin resistance, Mitochondrial dysfunction, Exercise training | ||
|mipnetlab= | |mipnetlab=NL Maastricht Schrauwen P | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Human | |organism=Human | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Permeabilized tissue | |preparations=Permeabilized tissue | ||
|injuries=Mitochondrial disease | |||
|diseases=Diabetes | |||
|instruments=Oxygraph-2k | |||
}} | }} | ||
Latest revision as of 16:37, 19 March 2015
| Phielix E, Meex R, Moonen-Kornips E, Hesselink MK, Schrauwen P (2010) Exercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individuals. Diabetologia 53:1714-21. |
Phielix E, Meex R, Moonen-Kornips E, Hesselink MK, Schrauwen P (2010) Diabetologia
Abstract: AIMS/HYPOTHESIS: We previously showed that type 2 diabetic patients are characterised by compromised intrinsic mitochondrial function. Here, we examined if exercise training could increase intrinsic mitochondrial function in diabetic patients compared with control individuals.
METHODS: Fifteen male type 2 diabetic patients and 14 male control individuals matched for age, BMI and VO(2max) enrolled in a 12 week exercise intervention programme. Ex vivo mitochondrial function was assessed by high-resolution respirometry in permeabilised muscle fibres from vastus lateralis muscle. Before and after training, insulin-stimulated glucose disposal was examined during a hyperinsulinaemic-euglycaemic clamp.
RESULTS: Diabetic patients had intrinsically lower ADP-stimulated state 3 respiration and lower carbonyl cyanide 4-(trifluoro-methoxy)phenylhydrazone (FCCP)-induced maximal oxidative respiration, both on glutamate and on glutamate and succinate, and in the presence of palmitoyl-carnitine (p < 0.05). After training, diabetic patients and control individuals showed increased state 3 respiration on the previously mentioned substrates (p < 0.05); however, an increase in FCCP-induced maximal oxidative respiration was observed only in diabetic patients (p < 0.05). The increase in mitochondrial respiration was accompanied by a 30% increase in mitochondrial content upon training (p < 0.01). After adjustment for mitochondrial density, state 3 and FCCP-induced maximal oxidative respiration were similar between groups after training. Improvements in mitochondrial respiration were paralleled by improvements in insulin-stimulated glucose disposal in diabetic patients, with a tendency for this in control individuals.
CONCLUSIONS/INTERPRETATION: We confirmed lower intrinsic mitochondrial function in diabetic patients compared with control individuals. Diabetic patients increased their mitochondrial content to the same extent as control individuals and had similar intrinsic mitochondrial function, which occurred parallel with improved insulin sensitivity. • Keywords: Type 2 diabetes, Insulin resistance, Mitochondrial dysfunction, Exercise training
• O2k-Network Lab: NL Maastricht Schrauwen P
Labels:
Pathology: Diabetes
Stress:Mitochondrial disease
Organism: Human
Tissue;cell: Skeletal muscle
Preparation: Permeabilized tissue
HRR: Oxygraph-2k
